Electroacupuncture with different current intensities can improve gastrointestinal motility in diabetic gastroparesis via vagal and sympathetic pathways.

BACKGROUND: Diabetic gastroparesis (DGP) disrupts gastric motility. Electroacupuncture (EA) at Zusanli (ST36) may alleviate DGP symptoms via neural pathways. AIM: To investigate how EA current intensities at ST36 regulate neural pathways and improve gastric motility in DGP models. METHODS: A DGP model was established using intraperitoneal injection of streptozotocin. Gastrointestinal motility was measured in rats after 2 weeks of continuous EA at ST36. Current intensity was selected as 0.5 mA, 1 mA, and 3 mA. Gastric electrodynamics were detected by recording and analyzing the number of gastric discharges. The gastric emptying rate and propulsion rate of the small intestine were measured to assess dynamic gastrointestinal function. Hematoxylin-eosin staining was conducted to measure histopathological changes in the gastric sinus. Reverse transcription-polymerase chain reaction was conducted to determine mRNA levels of Rho guanine nucleotide-binding protein A and Rho-associated coiled-coil forming protein kinase. Western blotting was conducted to determine the expression levels of choline acetyltransferase, tyrosine hydroxylase, Rho guanine nucleotide-binding protein A, and Rho-associated coiled-coil forming protein kinase. Immunofluorescence staining in the stomach was conducted to detect the distribution of C-kit, an interstitial cell of Cajal marker. An enzyme-linked immunosorbent assay was conducted to detect serum levels of acetylcholine and norepinephrine. RESULTS: Treatment with EA improved gastric emptying and gastric smooth muscle disorders in rats with DGP, mitigated pathological damage, and restored the function of interstitial cells of Cajal. In addition, different current intensities of EA affected gastrointestinal function of rats with DGP. The 0.5 mA, 1 mA, and 3 mA EA groups all improved gastrointestinal function. 0.5 mA EA increased acetylcholine levels by increasing protein expression of choline acetyltransferase (P < 0.05), thereby upregulating vagus nerve activity and enhancing parasympathetic nerve regulation. 3 mA EA increased norepinephrine levels (P < 0.05) by increasing protein expression of tyrosine hydroxylase, thereby activating the sympathetic nervous pathway. 1 mA coordinated the function of the vagus and sympathetic nerves to improve gastrointestinal motility. CONCLUSION: EA with ST36 improved gastric motility in rats with DGP. 0.5 mA EA activated the vagus nerve, while 3 mA EA regulated gastrointestinal motility by activating the sympathetic nerves.